Neuropathic pain is a major public health problem. Treatment for this disorder has had limited success owing to our incomplete understanding of the mechanisms that underlie the induction of neuropathic pain. Nerve injury-induced neuropathic pain is thought to be triggered by abnormal spontaneous activity that arises in neuromas and first-order sensory neurons of the DRG. The abnormal excitability may result from maladaptive changes in gene transcription and translation of receptors, enzymes and voltage-dependent ion channels in the DRG4. Voltage-dependent potassium channels govern cell excitability. Peripheral nerve injury downregulates expression of mRNA and protein for these channels in the DRG, a phenomenon that may contribute to induction of neuropathic pain. However, the molecular mechanisms that underlie this downregulation are still unknown.